New insights into hepatitis B virus biology and implications for novel antiviral strategies

Abstract

Abstract Hepatitis B virus (HBV), a small DNA virus with a unique replication mode, can cause chronic hepatitis (CHB), which is characterized by the persistence of the viral covalently closed circular DNA that serves as the template for HBV replication and the production of large amounts of secreted HBV surface antigen (HBsAg) that is present in excess of the levels of infectious virus. Despite the success of currently approved antiviral treatments for CHB patients, including interferon and nucleotide analogs, which suppress HBV replication and reduce the risk of CHB-related liver diseases, these therapies fail to eradicate the virus in most of the patients. With the development of the cell and animal models for HBV study, a better understanding of the HBV life cycle has been achieved and a series of novel antiviral strategies that target different stages of HBV replication have been designed to overcome the viral factors that contribute to HBV persistence. Such basic HBV research advancements and therapeutic developments are the subject of this review.